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Treating blood cell problems caused by short telomeres and aging by blocking damage signals at chromosome ends
Updated
Abstract
Targeting telomeric noncoding RNAs with telomeric antisense oligonucleotides (tASO) improves hematopoietic function in telomerase-deficient mice.
- Telomeres shorten and accumulate damage with aging, contributing to cellular senescence and hematopoietic dysfunction.
- Telomeric noncoding RNAs are synthesized in response to telomere dysfunction and are involved in the activation of the telomeric DNA damage response (tDDR).
- In telomerase-deficient mice, suppressing tDDR with tASO reduces senescence and inflammation in hematopoietic organs.
- Targeting tDDR alleviates hematopoietic dysfunction and enhances the fitness and repopulating potential of hematopoietic stem cells.
- Similar improvements were observed in aged wild-type mice and in human hematopoietic stem cells from aged donors after tASO treatment.
Simplified
Longevity & Aging